View clinical trials related to Muscle Weakness.
Filter by:Evaluate the long-term safety of amifampridine phosphate in patients with MuSK antibody positive and AChR antibody positive myasthenia gravis.
This study evaluates the effect of the addition of gait training to physical therapy on the gait of geriatric rehabilitation inpatients. Half of the patients will receive gait training with a gait training machine and conventional physical therapy in combination, the other half of the patients will receive conventional physical therapy alone.
This study will evaluate the safety and effectiveness of Respiratory-gated Auricular Vagal Afferent Nerve Stimulation (RAVANS) for improving motor recovery after stroke. Subacute stroke patients will receive RAVANS or sham stimulation concurrent with arm motor training during 10 intervention sessions occurring daily for 30 minutes over 2 weeks. The safety and improvements in arm motor function after the intervention will be compared in patients receiving RAVANS to those receiving sham stimulation.
This pilot research study is being done to see if the drug abatacept (Orencia ®) will be helpful in treating patients with myasthenia gravis (MG) who do not respond satisfactorily to other drugs that are used to suppress the immune system. Abatacept has been successful in treating experimental MG in laboratory animals, and this study is to determine its effectiveness in patients with MG.
This phase IIb randomized trial studies how well cholecalciferol (vitamin D3) supplementation works in strengthening inspiratory muscles in cholecalciferol-deficient patients with chronic obstructive pulmonary disease (COPD). Cholecalciferol supplementation may help reduce the risk of developing lung cancer and strengthen the diaphragm in cholecalciferol-deficient patients with COPD.
ICU acquired muscle weakness is a significant problem in patients recovering from critical illness. This trial will evaluate the safety and efficacy of a drug in improving muscle weakness in critically ill patients.
Spinal cord injury (SCI), especially involving the cervical and upper thoracic segments, can significantly compromise respiratory muscle function. Respiratory complications can ensue, including lung collapse and pneumonia, which are the primary cause for mortality in association with traumatic SCI both during the acute and chronic phases post-injury. Lesions at the level of the cervical or high thoracic spinal cord result in respiratory muscle weakness, which is associated with ineffective cough, mucus retention, and mucus plugging. Despite the fact that pulmonary complications are a major cause of morbidity and mortality in this population, there is a paucity of effective interventions in the SCI population known to improve respiratory muscle strength with pharmacologic interventions receiving little to no attention. The current objective of this study is to determine the effectiveness of 16 weeks of sustained release oral Albuterol to; (1) improve respiratory muscular strength, and (2) improve cough effectiveness.
Occlusion training, resistance exercise performed with a specialized venous tourniquet, leads to beneficial changes in muscle at low resistance and minimal stress on the nearby joint. This novel resistance training has the potential to greatly improve extremity muscle strength gains for rehabilitation patients who are unable for medical reasons to perform high resistance exercise. Our study will explore this with specific rehabilitation populations: post-operative knee scopes, post-operative anterior cruciate ligament (ACL) reconstruction patients who have acute post-operative changes in thigh muscle function and chronic thigh weakness. The primary outcome is to achieve accelerated functional thigh recovery with outcome measures including thigh strength, validated questionnaires, and validated functional testing. Occlusion training can enhance rehab patients outcomes, reduce the cost of care, and improve the skills and efficiency of care providers.
The main purpose for this study is to provide access to 3,4 DAP, a drug which has demonstrated to be effective in treating weakness associated with Lambert-Eaton Myasthenic Syndrome. LEMS is a rare autoimmune cause of a defect in neuromuscular transmission. The disorder is clinically characterized by fluctuating muscle weakness, hyporeflexia and autonomic dysfunction.
Pulmonary arterial hypertension (PAH) is a disease that causes raised blood pressure in blood vessels that pick up oxygen from the lungs. It has a life expectancy similar to some cancers. There is treatment available but there is no cure. We now know that PAH is associated with weakness in the muscles in the legs, which contributes to the symptoms patients' experience. Researchers believe that certain proteins found in high levels in the blood of patients with other chronic diseases can affect muscle function and growth. One of these proteins is called growth differentiating factor (GDF) 8, high levels of which are associated with muscle weakness in chronic obstructive pulmonary disease(COPD) and heart failure (HF). Interestingly there are drugs available which block the actions of GDF-8 on muscle cells which has been shown in animals to result in increased muscle size. A related protein called GDF-15 is found in elevated levels in patients PAH, and is linked to prognosis. Our preliminary data suggests that GDF-15 can also directly influence muscle size in a number of situations. We aim to investigate the role of GDF-15 and related molecules in the development of muscle weakness in patients with PAH. We will do this by measuring certain markers of muscle weakness and taking blood and muscle samples in patients and controls. We will then compare the levels of GDF-15 in these tissues in those with and without muscle wasting. We hope this work will lead to a greater understanding of the role of GDF-15 in the development of muscle weakness in patients with PAH. GDF-15 levels may be important in allowing us to define which patients have muscle weakness. In the future we aim to perform a clinical trial of drugs which block the actions of GDF-15.